Blockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells
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- Blockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells
- Shin, Hanho; Han, Ji Hye; Yoon, Juhwan; Sim, Hyo Jung; Park, Tae Joo; Yang, Siyoung; Lee, Eun Kyung; Kulkarni, Rohit N.; Egan, Josephine M.; Kim, Wook
- beta-cell function; cannabinoid 1 receptor; glucokinase; glucose transporter 2; insulin secretion
- Issue Date
- JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, v.22, no.4, pp.2337 - 2345
- Cannabinoid 1 receptors (CB1Rs) are expressed in peripheral tissues, including islets of Langerhans, where their function(s) is under scrutiny. Using mouse beta-cell lines, human islets and CB1R-null (CB1R(-/-)) mice, we have now investigated the role of CB1Rs in modulating beta-cell function and glucose responsiveness. Synthetic CB1R agonists diminished GLP-1-mediated cAMP accumulation and insulin secretion as well as glucose-stimulated insulin secretion in mouse beta-cell lines and human islets. In addition, silencing CB1R in mouse cells resulted in an increased expression of pro-insulin, glucokinase (GCK) and glucose transporter 2 (GLUT2), but this increase was lost in cells lacking insulin receptor. Furthermore, CB1R(-/-) mice had increased pro-insulin, GCK and GLUT2 expression in cells. Our results suggest that CB1R signalling in pancreatic islets may be harnessed to improve beta-cell glucose responsiveness and preserve their function. Thus, our findings further support that blocking peripheral CB1Rs would be beneficial to beta-cell function in type 2 diabetes.
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